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Environmental Exposure to Radioactive Iodine and Thyroid Disease

Wilkinson, Gregg S.

doi: 10.1097/01.ede.0000231373.60399.2c

From the University of Texas Medical Branch, Galveston, TX.

Address correspondence to: Gregg S. Wilkinson, Department of Preventive Medicine and Community Health, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1148. E-mail:

Few topics engender more vigorous debate than low-dose or chronic radiation effects on health, especially when exposures are due to the release of radioactive materials to the environment. Such releases have occurred as a result of nuclear weapons explosions, nuclear experiments and operations, and nuclear reactor accidents.

Concerns regarding effects to the thyroid from environmental radiation probably originated with the atomic blasts in Hiroshima and Nagasaki, and continued with the testing of ever more powerful atomic weapons during the Cold War years. The deliberate reactor releases at the Hanford Works in the state of Washington and accidents involving nuclear power plants, especially the Chernobyl catastrophe in the Ukraine, have further fanned the debate.

There has been particular concern about the atmospheric nuclear testing carried out at the Nevada test site. This concern led to a series of studies of thyroid disease and leukemia in populations residing in states surrounding the test site. Of special interest is the potential effect of iodine-131 (131I) on thyroid disease among those exposed during early childhood. To address this question, a cohort was assembled in 1965 consisting of children attending junior and senior high school in Washington County, Utah. This cohort has been examined every 5 years, including thyroid screening, collection of medical histories, and interviews of study subjects and their parents.1,2

Extensive efforts to estimate individual doses of 131I have been undertaken. Reports from this study have been published at various stages to describe both the dose reconstructions and assignment and results of the epidemiologic follow up (phases I and II).3–6 The report by Lyons and colleagues1 in this issue of Epidemiology is a revision (phase IIR) of the second epidemiologic follow-up study6 and the third in the series describing the dosimetry and epidemiologic results of the Utah cohort.

This revision was prompted by problems uncovered during preparations to implement phase III of the study. While gearing up for the new effort, a number of deficiencies were discovered, including corrupted data files, coding errors, software and hardware issues, dose-estimation errors, and problems of exposure and outcome misclassification.1,2 The researchers also used this opportunity to address another problem in the phase II results, namely that thyroid disease diagnoses had been assigned after exposures were known.1,8 In addition, the new analysis took advantage of new information from the National Cancer Institute (NCI) on estimated 131I thyroid doses to the U.S. populace from nuclear weapons tests fallout.7

The current report (phase IIR) corrects the deficiencies just mentioned and implements additional quality controls. The report revises the dose estimates (including application of the aforementioned NCI population dose estimates) to subjects who resided outside of Utah and surrounding states and who had previously been assigned doses of zero. Finally, the report uses data from rescreening subjects and assigns diagnoses using updated diagnostic criteria by clinicians who were blind as to exposure, residence, and other characteristics of the study subjects.1,2 To the authors’ credit, they present results from both the original and the revised analyses.

A potential issue is the manner of calculating dose estimates in the phase IIR study for those who lived outside the study catchment area. It appears the NCI dose calculator was used to estimate thyroid doses only for those who resided outside of the 7-state catchment area, whereas other data sources were used for those within the original 200-mile radius for which Nevada test site estimates were available. This needs to be clarified and perhaps consideration given to conducting a parallel analysis using the NCI calculator for the entire study population to assure similarity of assigned doses.

In general, the revised results are similar to the phase II results. As might be expected if nondifferential misclassification in phase II had diluted a true effect, the phase IIR risk estimates tend to be stronger. Dose–response trends are observed for all types of thyroid disease combined, thyroiditis, all thyroid nodules combined, all neoplasms combined, and for benign neoplasms but not for nonneoplastic nodules, thyroid cancers, or thyroiditis with hypothyroidism.

Rather than providing startling new findings, the revised results appear to be largely consistent with previous results with certain risk estimates being elevated.1

These results are generally consistent with the increased risks observed for Marshall Islanders9 and for children exposed to Chernobyl fallout10,11 but not with results from the Hanford study population8 for whom no association between 131I and thyroid disease has been observed.

This difference between Utah and Hanford study results deserves comment. The difference is probably not due to diagnostic bias12 in the revised Utah results, because the present effort took precautions to blind the case adjudication panel. The mean dose for the Hanford study population was higher (174 mGy) than for the Utah population (120 mGy overall) and thus would not explain the difference in outcomes.

Might there be unmeasured factors acting as effect modifiers in the 2 settings? Recently, Cardis et al11 reported results from a case–control study of 131I exposure from Chernobyl fallout and thyroid cancer in Belarus and the Russian Federation. The authors observed a linear dose–response between thyroid cancer risk and thyroid dose in children that was modified by the presence of stable iodine in soil or supplementation with potassium iodide. Perhaps consideration of environmental iodine or potassium iodine supplementation would help to explain differences in the Utah and Hanford studies.

Despite the large amount of research concerning radiation effects on the thyroid, there is much we do not know. The contribution by Lyons and his colleagues1 in this issue of Epidemiology adds to our knowledge and at the same time raises new questions that will continue to feed the controversy about environmental radiation and thyroid disease.

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GREGG S. WILKINSON is Professor of Epidemiology and Biostatistics in the Department of Preventive Medicine and Community Health at the University of Texas Medical Branch and Adjunct Professor at the University of Massachusetts School of Public Health. He has a longstanding research interest in the human health effects from exposures to low doses of ionizing radiation, especially exposures received in environmental and occupational settings.

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© 2006 Lippincott Williams & Wilkins, Inc.